To investigate the role and novel mechanism of Rab32 on the proliferation, migration, and invasion of non-small cell lung cancer (NSCLC) cells.

The expression of Rab32 in NSCLC was assessed using bioinformatics. The mRNA and protein expression levels of Rab32 in NSCLC cells were determined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. Stable Rab32-overexpressing A549 and H1299 cell lines were constructed using a lentivirus system, with the overexpression group serving as the observation group. The effects of Rab32 on the proliferation of NSCLC cells were evaluated by CCK-8 and colony formation assays. The impact of Rab32 on the migration and invasion capabilities of A549 and H1299 cells was examined using scratch and Transwell assays. The expression levels of epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, and Vimentin) in different groups of cells were measured by Western blot.

Bioinformatics analysis indicated that the mRNA expression of Rab32 was significantly reduced in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) compared to the control group(P<0.05). qRT-PCR and Western blot results revealed that the mRNA and protein expression levels of Rab32 in A549, H1299, and HCC827 were significantly lower than those in normal human bronchial epithelial cells (Beas-2B), with more pronounced decreases in A549 and H1299 cells. In A549 and H1299 cells, the mRNA and protein expression levels of Rab32 in the observation group were significantly higher than those in the empty vector control group (P<0.05). The CCK-8 and colony formation assay results showed that the cell proliferation and cloning capacity of the observation group were significantly reduced compared to the control group (P<0.05). The scratch and Transwell assay results suggested a marked decrease in the migration and invasion capabilities of the observation group cells (P<0.05). Western blot analysis showed that the protein expression level of the epithelial phenotype marker E-cadherin in the observation group cells was significantly higher than that in the control group, while the expression of mesenchymal phenotype markers N-cadherin and Vimentin was markedly increased compared to the control group (P<0.05).

Rab32 inhibits the proliferation, migration, and invasion of NSCLC cells and may serve as a potential new avenue for the clinical treatment of NSCLC patients.